IL-27 attenuates the TGF-β1-induced proliferation, differentiation and collagen synthesis in lung fibroblasts

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• 作者：Zhaoxing Dong^a ; ¹ ; ^{dongkm@hotmail.com" class="auth_mail" title="E-mail the corresponding author} ; Xinxiang Zhao^b ; ¹ ; ^{zhaoxinxiang06@126.com" class="auth_mail" title="E-mail the corresponding author} ; Wenlin Tai^c ; ^{2820582685@qq.com" class="auth_mail" title="E-mail the corresponding author} ; Wen Lei^a ; ^{2233851218@qq.com" class="auth_mail" title="E-mail the corresponding author} ; Yin Wang^a ; ^{w.y925@163.com" class="auth_mail" title="E-mail the corresponding author} ; ZhenKun Li^a ; ^{ljk5718@sina.com.cn" class="auth_mail" title="E-mail the corresponding author} ; Tao Zhang^a ; ^{ZT6958@sina.com.cn" class="auth_mail" title="E-mail the corresponding author}
• 关键词：LFs ; TGF-β1 ; Interleukin-27 ; Proliferation ; Differentiation
• 刊名：Life Sciences
• 出版年：2016
• 出版时间：1 February 2016
• 年：2016
• 卷：146
• 期：Complete
• 页码：24-33
• 全文大小：2527 K

文摘

Pulmonary fibrosis is a type of chronic lung disease and has characteristics that progress quickly, has a high fatality rate and a poor therapeutic effect. Our previous research showed that interleukin-27(IL-27) potentially attenuates BLM-induced pulmonary fibrosis, but the function of IL-27 in lung fibroblasts (LFs) differentiation pulmonary fibrosis is yet to be known.

Main methods

Here we investigated the effect of IL-27 on the proliferation, differentiation and collagen synthesis of lung fibroblasts induced by transforming growth factor-β1 (TGF-β1)using MTT, bromodeoxyuridine(BrdU) staining, real-time quantitative PCR(qPCR), Western blot, cell cycle FACS assay and immunofluorescence. We also examined the expression of the JAK/STAT and TGF-β1/Smad signaling pathway of IL-27 in lung fibroblasts.

Key findings

TGF-β1 treated lung fibroblasts showed significantly increased proliferation, differentiation and collagen synthesis as well as overactivated JAK/STAT and TGF-β1/Smad signaling. However, the presence of IL-27 weakened these effects and obviously inactivated the JAK/STAT and TGF-β1/Smad signaling pathways.

Significance

Our results indicate that IL-27 may play an anti-fibrotic role in the development, differentiation and collagen synthesis in lung fibroblasts. These data also may provide a target gene therapy method in treating pulmonary fibrosis.